Migraine aura consists of fully reversible focal neurologic symptoms that may precede or coexist with headache in a significant minority of migraine patients. Typical aura symptoms include visual, sensory, and language disturbances. The most recent International Classification of Headache Disorders, 3rd edition (beta version) has added other aura types such as brainstem localizing symptoms, lateralizing weakness, and monocular visual loss. Currently available data from animal models and functional neuroimaging in humans implicate cortical spreading depression (CSD) as the phenomenon underlying migraine aura. Ongoing study suggests that susceptibility to migraine aura and CSD may be genetically mediated. CSD appears to be a potential target for future development of migraine-specific preventive therapies.

Around 10 % of the global adult population has active migraine. The public health burden of migraine is high because migraine attacks are associated with temporary disability and substantial impairment in activities. As such, migraine is ranked as one of the most disabling conditions. The widespread disability produced by migraine is therefore an important target for treatment.

The hallmark of migraine is the head pain, but a plethora of other clinical symptoms is needed for a headache to be qualified as a migraine according to the current diagnostic criteria.

There has been tremendous progress in our acceptance, understanding and treatment possibilities of migraine, but to optimize migraine management, it is important that we continue to improve our understanding of the basic migraine mechanisms. An understanding of migraine pathophysiology must encompass the varied clinical symptoms and relate these findings to anatomy and physiology.

The headache research field is privileged to have in its preclinical laboratories well-established animal models that significantly facilitate and improve our understanding of headache mechanisms, in particular in terms of the molecular signalling and brain networks involved. A variety of pharmacological screening approaches for novel therapeutics and for the improvement of advanced pharmacological agents can be achieved in translational research utilising these models. The available migraine models have been developed based on our understanding of migraine from clinical, migraine patient-specific evidence. These clinical phenotypes have been successfully employed to model features of the disease physiology in animals and to provide reproducible meaningful physiological measures in the laboratory.

Cognitive dysfunction has recently gained attention as a significant problem among migraine sufferers. All of the clinical studies show poor cognitive performance during migraine attacks, though, the interictal data are conflicting. Migraineurs show impaired cognitive function interictally in most of the clinic-based studies. Population-based studies did not reveal a difference in cognitive functions between migraineurs and controls. The specific cognitive domains involved are information processing speed, basic attention, executive functions, verbal and non-verbal memory and verbal skills. Neurophysiological, imaging and pharmacological studies support clinical symptoms of cognitive impairment in migraine. Longitudinal studies do not suggest progressive cognitive decline over time in migraine patients. Preventive medications and comorbid disorders such as depression and anxiety can impact cognitive function, but cannot fully explain the cognitive impairment in migraine. In contrast to migraine, tension type or cluster headache are not associated with cognitive impairment, at least during headache-free periods.

Headache is the most common and one of the most disabling types of chronic pain among children and adolescents. At age 5, 20% of children have headache, and by the age of 15, the prevalence of headache may be as high as 82%. We now know more about headache than ever before. Our understanding of headache pathogenesis expanded considerably when the International Headache Society published good diagnostic criteria in 1988 and elaborated in 2004, unfortunately most of these criteria were developed for adults, not children, and therefore our knowledge of pediatric headache has lagged behind what we know about adult headache.Herein we discuss diverse types of pediatric headache, from migraine to the trigeminal autonomic cephalalgias, medication overuse headache, secondary headaches, and more. The issues of pathophysiology, epidemiology, acute and preventive treatment, and non-pharmacological treatments are discussed.The purpose of this chapter is to bring together current information on pediatric headache, recognizing that a more detailed discussion is not possible in this format, but perhaps the reader will be stimulated to explore further any topics of interest presented in this chapter.

Migraine, particularly migraine with aura has been associated with an increased risk of vascular events including ischemic and hemorrhagic stroke, myocardial infarction, and angina. Data also indicated that migraineurs, as compared to non-migraineurs, have an increased burden of infarct-like lesions and white matter abnormalities at brain magnetic resonance. There are no tools to identify the migraineurs who will suffer vascular events. Recent onset of the migraine, active migraine, and frequent attacks are features associated with the increased stroke risk; combined oral contraceptives and cigarette smoking may further increase the risk of ischemic stroke in migraineurs. The mechanisms underlying this increased vascular risk are still unclear but experimental studies indicated an increased cellular excitability in migraineurs that may make the brain tissue more susceptible to ischemia. Additionally, clinical data supported an impairment of the vascular function in migraineurs at the systemic level. There is currently no direct evidence to support that a migraine prophylactic treatment can reduce future stroke risk; however, we cannot exclude that migraine prophylaxis, by raising the threshold for spreading depolarization, may lower stroke risk.

Purpose of Review

A wide variety of triggers prompt attacks in episodic migraine. Although experimental triggers such as glyceryl trinitrate reliably produce migraine, natural triggers are much less predictable and vary in importance between individuals. This review describes the most common triggers in episodic migraine and provides strategies for managing them in clinical practice.

Recent Findings

Multiple migraine attack triggers have been established based on patient surveys, diary studies, and clinical trials. Stress, menstrual cycle changes, weather changes, sleep disturbances, alcohol, and other foods are among the most common factors mentioned. Clinical studies have verified that fasting, premenstrual periods in women, “letdown” after stress, and most likely low barometric pressures are migraine triggers. Premonitory symptoms such as neck pain, fatigue, and sensitivity to lights, sounds, or odors may mimic triggers.

Summary

Multiple studies clearly demonstrate triggers in episodic migraine, often related to change in homeostasis or environment. Many common migraine triggers are not easily modifiable, and avoiding triggers may not be realistic. Healthy lifestyle choices such as exercise, adequate sleep, stress management, and eating regularly may prevent triggers and transformation to chronic migraine over time.

Chronic migraine is a common and disabling complication of migraine with a population prevalence of about 2%. Emerging evidence suggests that episodic migraine and chronic migraine differ not only in degree, but also in kind. Compared with patients with episodic migraine, those with chronic migraine have worse socioeconomic status, reduced health-related quality of life, increased headache-related burden (including impairment in occupational, social, and family functioning), and greater psychiatric and medical comorbidities. Each year, approximately 2.5% of patients with episodic migraine develop new-onset chronic migraine (ie, chronification). Understanding the natural disease course, improving treatment and management, and preventing the onset could reduce the enormous individual and societal burden of chronic migraine, and thus, have become important goals of headache research. This review provides a summary of the history of nomenclature and diagnostic criteria, as well as recent studies focusing on the epidemiology, natural history, and burden of chronic migraine.

Purpose of Review

To review the pathophysiologic, epidemiologic, and clinical evidence for similarities and differences between migraine with and without aura.

Recent Findings

The ICHD-3 has recently refined the diagnostic criteria for aura to include positive symptomatology, which better differentiates aura from TIA. Although substantial evidence supports cortical spreading depression as the cause of visual aura, the role (if any) of CSD in headache pain is not well understood. Recent imaging evidence suggests a possible hypothalamic origin for a headache attack, but further research is needed. Migraine with aura is associated with a modest increase in the risk of ischemic stroke. The etiology for this association remains unclear. There is a paucity of evidence regarding treatments specifically aimed at the migraine with aura subtype, or whether migraine with vs without aura responds to treatment differently. Migraine with typical aura is therefore often treated similarly to migraine without aura. Lamotrigine, daily aspirin, and flunarizine have evidence for efficacy in prevention of migraine with aura, and magnesium, ketamine, furosemide, and single-pulse transcranial magnetic stimulation have evidence for use as acute treatments. Although triptans have traditionally been contraindicated in hemiplegic migraine and migraine with brainstem aura, this prohibition is being reconsidered in the face of evidence suggesting that use may be safe.

Summary

The debate as to whether migraine with and without aura are different entities is ongoing. In an era of sophisticated imaging, genetic advancement, and ongoing clinical trials, efforts to answer this question are likely to yield important and clinically meaningful results.

Headache disorders are a public health priority as they are associated with significant disability and psychosocial impairment worldwide [64, 83]. Migraine is currently recognized as one of the major causes of lost days from work and school every year, and it is also responsible for severe lifestyle restrictions [84, 85]. Twice as common as tension-type headache, migraine is the most frequent primary headache and accounts for 22 % of all headache diagnoses, whereas other unspecified headache types may be observed in 18 % of cases [84, 85].